Phorbol ester and calcium ionophore did notmodulate the expression of the transfected IL-2 gene in NIH-3T3 and HeLa cells, while these agents increased its expression in transfected BFS lymphoma T cells.

CIP alone had noinfluence on the basal release of IL-2 by NOB-1 cells, a T cell line that responds to IL-1 with an increase in IL-2 synthesis, but, in combination with recombinant IL-1, CIP significantly enhanced the release of IL-2 by these cells.

The expression of the IL-2 receptor (Tac) during T lymphocyte activation was notaltered by K channel blockers, whereas the production of interleukin 2 (IL-2) was reduced to the level in unstimulated T lymphocytes.

We conclude that PMA can stimulate IL-2 secretion independent of the translocation of PKC activity, and suggest that there is an alternative mechanism of action for phorbol esters in activated T cells.

Addition of the H-22.10 mAb at the initiation of such stimulated T-cell cultures was found to prevent the augmentation of TAP but not to affect the emergence of IL-2 receptors or the increase of Pgp-1 expression.

In our data set, however, the contribution of IL-2 from naïve CD8+ T cells in response to SEB stimulation is minimal compared to the antigen-experienced cells (not shown), and does notchange the relationship we observe between IL-2 and perforin.

To better define the cellular events that lead to the induction of anergy, we used the immunosuppressive agent rapamycin, which blocks T cell proliferation in late G1 phase but does notaffect costimulation-dependent IL-2 production.

In the present study, we have determined the comparative effects of two chemically distinct and endobronchially detectable QSSM, N-(3-oxododecanoyl)-L-homoserine lactone (3-oxo-C12-HSL) and 2-heptyl-3-hydroxy-4 (1H)-quinolone or the Pseudomonas quinolone signal (PQS), on human leukocytes exposed to a series of stimuli designed to detect differential immunological activity in vitro. 3-Oxo-C12-HSL and PQS displayed differential effects on the release of interleukin-2 (IL-2) when human T cells were activated via the T-cell receptor and CD28 (a costimulatory molecule). 3-Oxo-C12-HSL inhibited cell proliferation and IL-2 release; PQS inhibited cell proliferation withoutaffectingIL-2 release.

The experiments reported herein suggest that in general the T cell proliferation in AMLR is not completely dependent on the presence of IL-2 in the cultures and that aged subjects are probably defective in the production of other factor(s) presumably involved in AMLR proliferation, since the addition of exogenous IL-2 does not produce T-cell proliferation comparable to normal young subjects.

There was no significant difference in the production of IL-2 by patient and control T cells stimulated with plate-bound anti-CD3 at concentrations of 0 µg/ml, 0.01 µg/ml, 0.1 µg/ml and 1 µg/ml (figure 4A), demonstrating that insufficient IL-2 production is notresponsible for lower T cell proliferative responses observed in schizophrenia patients.

For splenocytes and LNL from flight (FLT) animals, IL-2 production decreased in response to the T cell receptor-independent mitogen 12-O-tetradecanoylphorbol-13-acetate plus ionomycin, but was notaffected by stimulation with the T cell receptor-dependent mitogens Concanavalin A or phytohemagglutinin.

Expression of B7-2 on these B cell populations was significantly higher than expression of B7-1 at all times assayed after stimulation; (c) blocking of B7-2 costimulatory activity inhibited TCR-dependent T cell proliferation and cytokine production, withoutaffecting early consequences of TCR signaling such as induction of CD69 or interleukin 2 receptor alpha (IL-2R alpha); and (d) expression of B7-1 and of B7-2 can be regulated by a variety of stimuli.

We found that lyso-PC increased IFN-gamma production and CD40L expression in CD4+ T cells stimulated with anti-CD3 Ab and recombinant CD80 molecules, whereas lyso-PC did notaffectIL-2 and IL-4 production.

Moreover, in PBMC-stimulated cultures exogenous IL-6 and IL-1 or antisera to these lymphokines did not significantly alter proliferative responses, cytotoxicity, IL-2 levels in the supernatant, or IL-2R expression on responder T cells.

Furthermore, these studies suggest that lymphokine production in T cells is notcontrolled by an "on/off" switch, but rather, that CD28 regulates a distinct intracellular pathway which modulates the level of IL-2 production on a per cell basis.

Antisense oligonucleotides corresponding to c-myc block the constitutive expression of c-Myc protein in T cell hybridomas and interfere with all aspects of activation-induced apoptosis withoutaffectinglymphokine production in these cells.

In this report, we show that 5-Fluorouracil increases the Interleukin-1 expression upto 2.66 folds without significantly affecting the levels of surface expression of p55 IL-2 receptor on human Peripheral blood mononuclear cells, CD4 and CD8 T cells.

When examined for their effects on cytokine production, CD3-dependent production of IL-2 and IFN-gamma was affected by neither cytokine, whereas IL-4 strongly inhibited the production of IFN-gamma by IL-2-stimulated T cells.

On coculture of "naive"CD4(+) T cells with mature DC in the presence of superantigen, ICOS was highly up-regulated on T cells, but played only a secondary role in the CD28-dominated release of TNF-alpha and IFN-gamma, and did notparticipate in the induction of IL-2.

We conclude that in patients with laryngeal carcinoma there is a phenotypic alteration of the T cells that is variable according to tumor stage, without functional alterations in blastogenic capacity or IL-2 production.

When peptide was administered i.v. without adjuvant, 50% of the Ag-specific cells expressed IL-2, but the peak of expression occurred before IL-2 receptor alpha-chain up-regulation, and only a minority of the Ag-specific T cells underwent blast transformation.

Unfractionated Con A supernatants, containing IL 2 and other factors known to influence T cell responsiveness, or IL 2-containing media of stimulated hybridomas affectneither the growth nor the lytic activity of the hybridomas.

RESULTS: The supernatant of the cultured non-immunological cells of decidua can inhibit the immunological function of T cells, natural killer cells and B cells to different extents, their maximum inhibiting ratio were 22.7%, 52.3% and 14.8% respectively, but there is no significant effect on the IL-2 secretion by lymphocytes.

More interestingly, while we have also observed increased activation and proliferation by human T cells upon culture with RAR agonists, no significant changes in the production of IL-2 (another type 1 cytokine) were observed post RAR agonist treatment in our hands (data not shown).

In addition, we have found that wortmannin, a potent inhibitor of PI3 kinase, does notinterfere with the induction of IL-2 after stimulation of Jurkat T cells with anti-CD28 monoclonal antibody and PMA.

In this study, we show that adenosine suppressed IL-2-dependent proliferation of CTLL-2 T cells by inhibiting STAT5a/b tyrosine phosphorylation that is associated with IL-2R signaling withoutaffectingIL-2-induced phosphorylation of Jak1 or Jak3.

During UVA1-triggered immediate apoptosis of Jurkat T cells, IFN-gamma levels increased in a dose-dependent manner at 4 h, but returned to baseline levels at 24 h post-exposure, whereas, there was no significant change in IL-2 at 4 or 24 h.

The antagonists based on the neurotensin-VIP hybrid molecule did notaffect the inhibitory effect of VIP/PACAP on IL-2 and IL-10 production, confirming that astrocytes and T lymphocytes express different receptors.